Description
Cholangiocarcinoma is a cancer of the hepatic bile ducts that is typically detected at a stage too advanced for resection. Additionally, chemotherapy is of limited efficacy, hence, novel therapeutic approaches are urgently required, including targeting of the cancer stroma. A macrophage-derived signal, tumour necrosis factor-like weak inducer of apoptosis (TWEAK), binds to cell-surface fibroblast growth factor-inducible 14 (Fn14), on cholangiocarcinoma cells to induce cytokine and chemokine expression and secretion. These TWEAK-inducible factors from cholangiocarcinoma cells can also affect macrophage polarisation. We characterised proteins secreted by four well-characterised human cholangiocarcinoma cell lines in the presence or absence of recombinant human TWEAK (100 ng/ml), to discover novel TWEAK-inducible factors that could drive pro-tumour niche formation.
[doi:10.25345/C56940]
[dataset license: CC0 1.0 Universal (CC0 1.0)]
Keywords: Cholangiocarcinoma, niche, stroma, TWEAK, Fn14, inflammation
Contact
Principal Investigators:
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Prof.Stuart Forbes, MRC Centre for Regenerative Medicine, Little France Drive, University of Edinburgh, EH16 4UU, United Kingdom
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domthe
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Publications
Dwyer BJ, Jarman EJ, Gogoi-Tiwari J, Ferreira-Gonzalez S, Boulter L, Guest RV, Kendall TJ, Kurian D, Kilpatrick AM, Robson AJ, O'Duibhir E, Man TY, Campana L, Starkey Lewis PJ, Wigmore SJ, Olynyk JK, Ramm GA, Tirnitz-Parker JEE, Forbes SJ.
TWEAK/Fn14 signalling promotes cholangiocarcinoma niche formation and progression.
J Hepatol. Epub 2020 Nov 19.
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Distinct protein accessions are counted across all files submitted in the "Statistical Analysis
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